Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Individuals with epilepsy commonly experience memory loss. We investigated the safety and tolerability of galantamine in treatment of memory loss in a pilot study of 28 patients with epilepsy, randomly assigned to galantamine (n=13) or placebo (n=15) and followed for a total of 12 weeks. Participants underwent blinded memory assessment at baseline and 12 weeks (Selective Reminding Test, 7/24 Spatial Recall). One participant in the galantamine group had a suspected recurrence of brain neoplasm and increased seizures; all other participants receiving galantamine showed no increase in seizure activity during the trial. Patients in both groups reported mild, tolerable side effects (headache, appetite suppression), with no difference between groups. No significant differences were observed on the memory measures when both groups were retested at Week 12. Galantamine appears to be safe and tolerable in patients with epilepsy. Further studies with larger samples and comparison with other cholinesterase inhibitors should be considered.
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PMID:The safety and tolerability of galantamine in patients with epilepsy and memory difficulties. 1855 48

We detected infection with a Bartonella species (B. henselae or B. vinsonii subsp. berkhoffii) in blood samples from six immunocompetent patients who presented with a chronic neurological or neurocognitive syndrome including seizures, ataxia, memory loss, and/or tremors. Each of these patients had substantial animal contact or recent arthropod exposure as a potential risk factor for Bartonella infection. Additional studies should be performed to clarify the potential role of Bartonella spp. as a cause of chronic neurological and neurocognitive dysfunction.
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PMID:Bartonella sp. bacteremia in patients with neurological and neurocognitive dysfunction. 1863 3

Human herpesvirus (HHV) 6, the etiologic agent of roseola, is nearly universally acquired during childhood. The virus establishes lifelong infection, including within the central nervous system (CNS), and replicates within several CNS cell types. HHV-6 has been linked to CNS disease during primary infection, including febrile seizures and possibly hippocampal injury. HHV-6 may also be associated with neurologic disease later in life, particularly in transplant patients. Recent reports offer evidence that HHV-6 reactivation may underlie a characteristic limbic encephalitis syndrome following hematopoietic cell transplant; the cardinal features of this syndrome include memory loss, insomnia, electroencephalographic evidence of temporal lobe seizure activity, MRI signal intensity abnormalities of the mesial temporal lobe, and the syndrome of inappropriate release of antidiuretic hormone. HHV-6 DNA is frequently detectable by nucleic acid amplification tests in the cerebrospinal fluid and peripheral blood upon symptom onset, which may provide a screening strategy in high-risk patients. Possible associations of HHV-6 with meningoencephalitis, mesial temporal lobe epilepsy, and multiple sclerosis in apparently immunocompetent hosts are under investigation.
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PMID:Human herpesvirus 6 encephalitis. 1876 2

Neurological manifestations may complicate Takayasu arteritis (TA) but seizures are rare. A 40-year-old man with TA presented with recurrent episodes of epileptic seizures. Episodes consisted of a brief period of unresponsiveness followed by sudden falling, tonic stiffening and limb jerking. A postictal period with drowsiness, urine incontinence and a temporal loss of memory was also present. A carotid and intracranial duplex ultrasound revealed a reverse flow within the left vertebral artery indicating the presence of subclavian stealing syndrome while extracranial MRA suggested some stenosis at the origin of the left common carotid artery. The EEG was consistent with epilepsy. Neurological manifestations are secondary to ischemia caused by decreased blood flow in the involved carotid and vertebral arteries. Antiepileptic treatment proved effective and may be considered as a reasonable first approach. The stenotic lesions can be managed successfully with angioplasty but these procedures are associated with a high failure rate and may not be needed.
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PMID:Takayasu arteritis presenting as epileptic seizures: a case report and brief review of the literature. 1894 53

Limbic encephalitis is a multifocal inflammatory disorder characterized by personality changes, irritability, memory loss, seizures, and, in some cases, dementia. In many cases, it may occur as a paraneoplastic syndrome and therefore the diagnosis of limbic encephalitis should raise the possibility of occult malignancy. We present a case of limbic encephalitis associated with a thymic carcinoid tumor. To our knowledge the association of thymic carcinoid tumor with paraneoplastic limbic encephalitis has not previously been reported.
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PMID:Paraneoplastic limbic encephalitis due to thymic carcinoid. 1905 77

Endoscopic third ventriculostomy (ETV) is a well established treatment for selected cases of obstructive hydrocephalus. However, it does carry a significant rate of failure, which can be abrupt and life threatening. The present study analyses the benefits versus the risks of routine CSF reservoir insertion during ETV. Clinical data obtained from the medical records of patients from a single neurosurgical centre who underwent ETV between August 2002 and February 2007 were analysed retrospectively. A total of 34 records were available with follow-up ranging from 3-56 months (Median 26 months) and with patient age range between 6 months - 75 yrs (median 19 years). During this period, one neurosurgeon routinely placed reservoirs in all patients undergoing ETV (n = 34). In all instances of reservoir insertion, Ommaya reservoirs were used. The number of patients in which the reservoir was tapped for diagnostic and/or therapeutic reasons was quantified, and all complications resulting from reservoir placement recorded. ETV success was defined by a lack of subsequent need for cerebrospinal fluid diversion. In total 13 of 34 (38%) reservoirs inserted were tapped at a later date and there were no complications associated with their insertion. Tapping of reservoirs helped determine which patients required subsequent ventriculoperitoneal (VP) shunting. In at least one case reservoir tapping was carried out as an emergency and was a crucial intermediate intervention prior to further surgery. The overall success rate of ETV was 65% (95% CI, 49-81%) with four complications associated with ETV: short-term memory loss, psychosis, and two cases of post-operative seizures. These complications were not attributed to CSF reservoir insertion but the ETV procedure itself. The routine placement of CSF reservoir following ETV thus seems justified with respect to the observed benefits and lack of complications associated with its placement.
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PMID:Is the routine placement of a CSF reservoir following endoscopic third ventriculostomy justified? 1966 81

Encephalitis with anti-NMDA receptor antibodies is a recently-recognised form of paraneoplastic encephalitis characterized by a prodromal phase of unspecific illness with fever resembling viral disease, followed by memory loss, psychiatric features, seizures, disturbed consciousness, prominent abnormal movements and autonomic imbalance. Association with ovarian teratoma is common. Neurological outcome can be good, especially when surgery is performed at an early stage. Here, we report a case of anti-NMDA receptor encephalitis associated with ovarian teratoma presenting with inaugural complex partial status epilepticus. The nature of abnormal movements at early stages was unclear and abnormal movements were misinterpreted as the recurrence of partial epileptic seizures. Despite its rarity, all clinicians treating epilepsy and movement disorders should be familiar with anti-NMDA receptor encephalitis, that appears to be a very severe but curable disease.
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PMID:Complex partial status epilepticus revealing anti-NMDA receptor encephalitis. 1973 68

Domoic acid (DA), the cause of Amnesic Shellfish Poisoning, is a naturally occurring marine biotoxin that is usually produced by the microscopic algae Pseudo-nitzschia. As is the case for other types of toxic algae, Pseudo-nitzschia outbreaks are becoming more frequent. Acute high-dose symptomology in humans includes vomiting, cramping, coma and death as well as neurological effects such as hallucinations, confusion and memory loss. Experimental studies and medical reports have collectively shown that DA exposure primarily affects the hippocampal regions of the brain and is associated with seizures and the disruption of cognitive processes. The neurobehavioral signature of DA is unique in that it includes transient and permanent changes in memory function that resemble human antegrade amnesia. Experimental studies with adult nonhuman primates have established that DA is a dose-dependent emetic that produces clinical and neuropathological changes consistent with excitotoxicity. Behavioral evaluations of treated rodents have shown that hyperactivity and stereotypical scratching are the first functional markers of toxicity. Mid-dose treatment is associated with memory impairment and behavioral hyperreactivity, suggesting changes in arousal and/or emotionality. At higher doses, DA treatment results in frank neurotoxicity that is characterized by seizures, status epilepticus and death in treated animals. The route of DA exposure is important and influences the severity of effects; intraperitoneal and intravenous treatments produce classic signs of poisoning at significantly lower doses than oral exposure. While developmental studies are few, DA readily crosses the placenta and enters the fetal brain. Domoic acid is not associated with congenital dysmorphia but is linked to persistent changes in motor behavior and cognition in exposed offspring. Comparative research suggests that functional losses associated with DA can be persistent and injuries to the CNS can be progressive. Long-term studies will be necessary to accurately track the expression of DA-related injury, in health and behavior, over the lifespan.
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PMID:Domoic acid: neurobehavioral consequences of exposure to a prevalent marine biotoxin. 1979 96

Why do complex-partial seizures in temporal lobe epilepsy (TLE) cause a loss of consciousness? Abnormal function of the medial temporal lobe is expected to cause memory loss, but it is unclear why profoundly impaired consciousness is so common in temporal lobe seizures. Recent exciting advances in behavioral, electrophysiological, and neuroimaging techniques spanning both human patients and animal models may allow new insights into this old question. While behavioral automatisms are often associated with diminished consciousness during temporal lobe seizures, impaired consciousness without ictal motor activity has also been described. Some have argued that electrographic lateralization of seizure activity to the left temporal lobe is most likely to cause impaired consciousness, but the evidence remains equivocal. Other data correlates ictal consciousness in TLE with bilateral temporal lobe involvement of seizure spiking. Nevertheless, it remains unclear why bilateral temporal seizures should impair responsiveness. Recent evidence has shown that impaired consciousness during temporal lobe seizures is correlated with large-amplitude slow EEG activity and neuroimaging signal decreases in the frontal and parietal association cortices. This abnormal decreased function in the neocortex contrasts with fast polyspike activity and elevated cerebral blood flow in limbic and other subcortical structures ictally. Our laboratory has thus proposed the "network inhibition hypothesis," in which seizure activity propagates to subcortical regions necessary for cortical activation, allowing the cortex to descend into an inhibited state of unconsciousness during complex-partial temporal lobe seizures. Supporting this hypothesis, recent rat studies during partial limbic seizures have shown that behavioral arrest is associated with frontal cortical slow waves, decreased neuronal firing, and hypometabolism. Animal studies further demonstrate that cortical deactivation and behavioral changes depend on seizure spread to subcortical structures including the lateral septum. Understanding the contributions of network inhibition to impaired consciousness in TLE is an important goal, as recurrent limbic seizures often result in cortical dysfunction during and between epileptic events that adversely affects patients' quality of life.
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PMID:Consciousness and epilepsy: why are complex-partial seizures complex? 1981

A 34-year-old woman with systemic lupus erythematosus (SLE) presented with general fatigue, seizures and memory loss. Magnetic resonance imaging of the brain showed a high signal area in the mesial temporal lobe bilaterally. Computed tomography scan of the chest and abdomen and ultrasound of pelvis detected no malignancy and tumour marker, antibodies to antineuronal antibodies (anti-Hu, anti-Ta and anti-Ma) and antibodies to voltage-gated potassium channels were all negative. The present case is limbic encephalitis (LE) associated with SLE and the pathogenesis may include autoimmunity shared. Our experience indicates that the immunologic spectrum of LE will expand to include additional immune mechanisms.
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PMID:Limbic encephalitis associated with systemic lupus erythematosus. 1985 Jun 55


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